Chronic periodontal disease has been characterized by gingival inflammation, soft tissue destruction and bone resorption. Studies have demonstrated that as a periodontal lesion evolves from an "initial" lesion to an "established" lesion, the cell population associated with each stage also changes. The initial lesion is characterized by a mixture of T and B lymphocytes, whereas the established lesion is marked by a predominance of plasma cells. Plasma cells secrete antibodies extravascularly in the connective tissues and in junctional epithelium in response to bacteria which constitute dental plaque. The continued presence of plaque could lead to the formation of immune complexes composed of bacterial antigens and antibodies which can elicit an inflammatory response. I am currently working with an in vitro model which explores the ability of accessory cells and immune complexes to regulate B cell function. One type of accessory cell, the macrophage, can take up immune complexes and in conjunction with prostaglandin secretion, induces an antigen specific B cell unresponsiveness. Thus, these B cells are unable to differentiate into plasma cells. Utilization of this model could elucidate a mechanism through which B cells function may selectively be turned off. Regulation of the host response by suppressing B cell function might prove a novel approach for ameliorating the pathogenesis of periodontal disease.